
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FADS6 CRISPR Activation Plasmid (m) | sc-435879-ACT | 20 µg | $397.00 |
Mouse Fads6 encodes FADS6, a putative fatty acid desaturase implicated in lipid metabolic homeostasis and the remodeling of cellular membrane phospholipids. As part of broader fatty acid desaturation and elongation networks, FADS6 may influence the balance of saturated and unsaturated fatty acids that shape membrane fluidity, organelle function, and lipid-mediated signaling. Altered desaturase activity is frequently linked to shifts in inflammatory tone, oxidative stress sensitivity, and metabolic adaptation in tissues with high lipid flux. Consequently, Fads6 is of interest for studying pathway-level regulation of lipid handling in metabolic and neuroimmune contexts relevant to complex disease biology.
FADS6 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Fads6 expression without altering the underlying DNA sequence.
FADS6 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Fads6 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the Fads6 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FADS6 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Fads6 locus and enabling the study of FADS6-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FADS6 pathway restoration in tumor cells with silenced or reduced Fads6 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.